Heparin acts on which pathway

Plasminogen itself will deposit on fibrin strands, waiting to be activated, by the activated factors circulating in the blood. Only plasminogen that has been absorbed by fibrin will be activated by the activators, I guess that by joining to fibrin there is a structural change exposing the active site , and plasminogen that escapes to the general circulation is broken down by its inhibitors, particularly PAI.

Fibrinolytic drugs e. These are still relatively new and used with caution. It should not be used to treat DVT the risks outweigh the benefits, although it may still rarely be used and is mainly only used to treat MI. In some cases it may be used to treat a massive PE. Reteplase — this is basically a modified synthetic tPA — it has reduced affinity for fibrin and fibrinogen, and normal affinity for PAI, but has increased duration of action.

Tenectplase — another synthetic tPA, it has increased affinity for fibrin, and reduced affinity for PAI which is good! Streptokinase — this is a bit different. It is produced by streptococcal bacteria. Pharmacokinetics They are all administered IV or intra-arterially. Streptokinase — some is removed by streptococcal antibodies before it forms its complex. Once it has formed its complex it is broken down enzymatically. Haemorrhage — is usually minor, but can occasionally be serious, eg.

Intracerebral haemorrhage. Other haemorrhagic complications may involve GI bleeds and stroke. It occurs slightly more frequenctly with the —plases compared to streptokinase. Hypotension — this is dose related and is most common with streptokinase. It is possibly a result of release of bradykinin release which is a result of unbound streptokinase circulation. The blood pressure will rapidly return to normal if the treatment is stopped for a short while.

Allergy — These are very rare, and only really occur with streptokinase as a result of its bacterial origin. In MI the sooner you give the drugs, the greater their effects. You should try to ensure they administered before 12 hours after the onset of symptoms. Trials have shown that the drugs are all pretty much equal in their efficacy, but that mechanical opening of the affected artery is more effective than using thrombolysis.

MI — use only when there is ST segment elevation, and symptom duration is less than 12 hours. Tranexamic acid — inhibits plasminogen activation, and thus prevents fibrinolysis. However, the tPA binding action odes then not cause activation of plasminogen, and thus plasminogen will not act on fibrin. Can cause nausea, diarrhoea and vomiting. Aprotinin — this is a broad spectrum protease inhibitor. It has many effects, including:. For both of these drugs, the theoretical risk of thrombotic tendency does not appear to be a clinical issue.

Tags: Clotting , Haematology. After graduating from his medical degree at the University of Manchester in , Tom completed his Foundation Training at Bolton Royal Hospital, before moving to Australia in He started almostadoctor whilst a third year medical student in Read full bio.

Jack 8 Jul Reply. This article as that mixed around. Thanks Jack, I have fixed this up, Tom. David 10 Jun Reply. Leave a Reply Cancel reply. Search this website Type, then hit enter to search. Type your search. Nov 19, Share this: Twitter Facebook.

More pathology! Eva on November 24, at pm. Brilliant, thanks! Kristine on November 25, at pm. Glad to help. Stephen Garramone, M. Julie on January 23, at am. Kristine on January 23, at pm. Nice explaination. It realy helped me. Michael Z. Johny on September 4, at pm. Thanks so much for your simple but brilliant explanation ….

Heba on June 14, at am. Islam on April 20, at am. Ledo on April 11, at am. That is quite helpful. Veritas1 on May 30, at pm. Very clear explanation. Connor on June 8, at pm. Textbook quality explanation. Thank you very much!!! Lizzy on August 7, at pm. Factor IX and X have an effect early on in the intrinsic pathway.

Inhibiting Factor X has a double effect on the extrinsic pathway because if there is still some factor VII in the blood stream it will have no factor X to react with. Hence, it is very unlikely that any Xa and V will be formed to carry on the pathway towards the stable fibrin clot. The inhibition of Prothrombin then has an effect on the production of Thrombin and hence the clot as well. Overall the inhibition of these 4 factors has a major effect on the ability of the body to form a stable fibrin clot.